IL-1 receptor regulates S100A8/A9-dependent keratinocyte resistance to bacterial invasion

B. S. Sorenson, A. Khammanivong, B. D. Guenther, K. F. Ross, M. C. Herzberg

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

Previously, we reported that epithelial cells respond to exogenous interleukin (IL)-1α by increasing expression of several genes involved in the host response to microbes, including the antimicrobial protein complex calprotectin (S100A8/A9). Given that S100A8/A9 protects epithelial cells against invading bacteria, we studied whether IL-1α augments S100A8/A9-dependent resistance to bacterial invasion of oral keratinocytes. When inoculated with Listeria monocytogenes, human buccal epithelial (TR146) cells expressed and released IL-1α. Subsequently, IL-1α-containing media from Listeria-infected cells increased S100A8/A9 gene expression in nave TR146 cells an IL-1 receptor (IL-1R)-dependent manner. Incubation with exogenous IL-1α decreased Listeria invasion into TR146 cells, whereas invasion increased with IL-1R antagonist. Conversely, when S100A8/A9 genes were knocked down using short hairpin RNA (shRNA), TR146 cells responded to exogenous IL-1α with increased intracellular bacteria. These data strongly suggest that infected epithelial cells release IL-1α to signal neighboring keratinocytes in a paracrine manner, promoting S100A8/A9-dependent resistance to invasive L. monocytogenes.

Original languageEnglish (US)
Pages (from-to)66-75
Number of pages10
JournalMucosal Immunology
Volume5
Issue number1
DOIs
StatePublished - Jan 2012

Bibliographical note

Funding Information:
This study was supported by grant R01DE11831 to M.C.H. from The National Institutes of Health. The National Institute of Dental & Craniofacial Research provided fellowship support through F30DE020210 (B.S.S.) and T32DE007288 (B.S.S. and A.K.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIDCR or the NIH. We would like to thank Tim Jernberg and Chantrakorn Champaiboon for their assistance in creating the TR146 shRNA clones. We would like to acknowledge the assistance of the Flow Cytometry Core Facility of the Masonic Cancer Center, a National Cancer Institute designated comprehensive cancer center supported in part by P30CA77598.

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